A distinct area of maxillary alveolar tenderness is consistently noted in patients with headache: vascular, tension-type, post-traumatic, even in the headache-free state (asymptomatic patients)(1). This area has consistently been identified in patients suffering from facial pain (2) or posterior cervical muscle hyperactivity (spasm)(3). This zone of tenderness, usually absent or minimal in the normal state (2), occurs in the maxillary third molar apical area (FIG. 1) even if edentulous, and correlates closely with a plexus formed by the posterior superior alveolar branch of the maxillary nerve (FIG. 2, arrows).
In preliminary data analysis, 1026/1100 (93.2%) mostly asymptomatic migraine patients exhibited maxillary alveolar tenderness, with laterality and degree of tenderness closely related to laterality and severity of symptoms. This consistent finding has been corroborated by several neurologists.
In a pilot study of thirty asymptomatic migraine patients with a unilateral history, blinded, inexperienced examiners selected the symptomatic side in 27/30 (90%) patients, based on the laterality of intraoral palpation findings.
The following evidence associates this tender area with a localized inflammation:
In 18 consecutive patients with atypical facial pain (recently reclassified as facial pain, (International Headache Society) (4), ipsilateral tenderness and increased temperature were found in 15 and 17 patients, respectively; in two control groups, often patients, no significant association was observed between the area associated with maxillary tenderness and increased temperature (1). A YSI (Yellow Springs International) Model 43TA tele-thermometer covered by a disposable plastic sheath was used bilaterally to record temperatures (2),
A similar experiment (intraoral palpation, temperature recording) was performed on 40 patients during unilateral episodic migraine or tension-type headache in the departments of Neurology, Dentistry, Emergency Medicine (Westchester Medical Center, Valhalla, N.Y.) a private practice limited to oromandibular dysfunction (MHF, Mt. Vernon, N.Y.), and Our Lady of Mercy Hospital (Bronx, N.Y.). The posterior maxillary molar periapical areas were palpated bilaterally for tenderness, and their temperatures were recorded, as in the previously described facial pain experiment (2). Significant correlations were found between severity and laterality of symptoms to tenderness, and between temperature and tenderness differentials. Kappa statistics demonstrated good agreement between laterality of temperature differential and tenderness, and laterality of highest temperature and symptoms (1).
An intraoral vasoconstriction device was used on 12 patients with cervical pain and muscle spasm. Ice water circulating through hollow metal tubes shaped to fit the maxillary area of tenderness was held intraorally for 15 minutes on this area of tenderness, on these 12 patients. In 9 of these individuals, reduced cervical pain perception, upper trapezius electromyography signal reduction, and increased range of motion was produced. Six out of 12 individuals had accompanying headache, which was reduced or eliminated in 4 cases (3). This device, as used in the maxillary area of tenderness, has been cleared by the U.S. Food and Drug Administration for muscle spasm reduction (K955529).
In the emergency departments at Westchester Medical Center and Sound Shore Medical Center, 25 acute migraine and tension-type, headache patients were similarly treated by intraoral chilling, for 40 minutes. Treatment was supervised by eight non-blinded emergency medicine physicians. Patient ratings of pain (all patients) and nausea (migraine patients only), on a scale from 1 to 10, (10=most severe) pre- and post-treatment and 24 hours post-treatment ratings were recorded. Initial baseline and immediate post-treatment headache intensities were 7.7 and 3.0 respectively. Baseline and post-traumatic nausea intensities (19 migraine patients only) were 5.9 and 1.6 respectively. The mean reduction in headache score was 4.7 (p&lt;0.0005), and that for nausea was 4.3 (p&lt;0.005). No side-effects were reported or observed. Of the 25 patients, the 19 who were able to be followed for up to 24 hours showed a further significant decrease in pain, but not in nausea. No medications were given to the 20 patients whose headaches were relieved or eliminated by the 40 minute treatment. This local vasoconstrictive effect is in contrast to the systemic vasoconstriction produced by the specific anti-migraine medications.
Results of this study also demonstrated the effectiveness of application of intraoral circulating ice water applied to the posterior maxillary area for resolving symptoms related to head and neck pain (cervical pain and muscle spasm) secondary to neurogenic inflammation. Nine of 12 patients with cervical pain and muscle spasm treated for 15 minutes showed reduced cervical pain perception, upper trapezius electromyography signal reduction, and increased cervical range of motion. Findings from this study suggest a strong trigemino-cervical relationship to head and neck pain and headache.
Other studies have also suggested that a strong connection exists between trigeminal and cervical motor and sensory responses.
These experiments suggest that the intraoral marker, (area of maxillary alveolar tenderness), for the above pain disorders, is a local inflammation, associated with increased local blood flow (vasodilation) and edema. The increased local temperature and tenderness are classic signs of inflammation, and the significant response to local cooling is caused by edema (swelling, another classical sign of inflammation) resolution.
The treatment location is also significant. The maxillary alveolar tenderness is located in an area that permits access to the trigeminal system where it is unprotected by skin or bone. In a recent experiment, somatosensory trigeminal evoked potentials (STEP) were done on 12 healthy volunteers with no history of head or neck pain. The electrical input point was over the left infraorbital foramen. After a base-line STEP, low power helium-neon laser (1.7 mW, 632.5 nm, 50 Hz) was applied by light tissue contact, to the left apical third molar area for two minutes. This resulted in an immediate average STEP amplitude reduction of 61%, with further reduction of 65.2 and 71.8%, ten and 20 minutes later. These results, far in excess of any analgesic intervention studies, demonstrate significantly greater amplitude reduction than that produced by 150 mg Demerol.